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Biomedical subjects

G Davidai

Publications and source records attributed to G Davidai.

At least 19 recordsLinked to original sources
PubMed2004

Acetaminophen in the treatment of headaches associated with dipyridamole-aspirin combination.

The authors assessed the prevalence of headaches following extended-release dipyridamole/aspirin combination (DAC), and the efficacy of acetaminophen in the treatment of these headaches. Following DAC, 38.7% of the participants developed headaches. The headaches were self-limited (69.4% placebo efficacy in 2 hours) and the incidence markedly declined over time. Acetaminophen was no more effective than placebo in the acute and preemptive treatment of these headaches.

Acetaminophen↗
PubMed1996

Change in trabecular architecture as measured by fractal dimension.

The objective of this work was to expose dried trabecular bone material to a decalcifying environment and to quantify the change in the spatial distribution of the bone with a fractal measure. Digitized radiographic images were produced from four separate slices of human vertebral bone as they dissolved within a solution of nitric acid. Pixel data from a region of interest (ROI) within the trabecular bone were used to estimate the time-dependent change in fractal dimension of the ROI as the bone dissolved. Results demonstrated that a change in the spatial distribution of trabecular material may be expressed in terms of a concurrently changing estimate of the fractal dimension.

Algorithms↗
PubMed1996

Middle cerebral artery velocity correlates with nitroglycerin-induced headache onset.

Headache often accompanies treatment with nitroglycerin, but the cerebral hemodynamic effects and the exact mechanism of the headache are incompletely understood. Transcranial Doppler monitoring allows evaluation and monitoring of changes in blood flow velocity in the large intracranial arteries. The objective of this study was to assess middle cerebral artery (MCA) blood flow velocities with transcranial Doppler monitoring in subjects receiving continuous low-dose nitroglycerin intravenously or by patch, and correlate these with clinical headache. Twenty-eight normal adult men received nitroglycerin (0.12 micrograms/kg/min intravenously [n = 14] or 0.6 mg/min by transdermal patch [n = 14]), for up to 120 minutes, with monitoring of clinical headache status (standard 4-point scale), blood pressure, heart rate, end-expiratory PCO2 (CO2), and right MCA velocity. All subjects developed headache (mean time to onset, 34 min), reaching moderate or severe levels in 20. There were no differences in age, weight, mean blood pressure, mean heart rate, or resting end-tidal CO2 between those whose headache reached a moderate to severe level and those whose headache remained mild. MCA velocity decreased from baseline values at all levels of clinical headache (onset, -17%; moderate, -18%; severe, -16%; nitroglycerin stopped, -19%) (p, 0.0001 by t test for each stage of headache). MCA velocity remained decreased at the time of headache resolution (-14%; p < 0.001). Blood pressure, heart rate, and CO2 did not change significantly. There were no differences related to route of nitroglycerin dosing. These data show that continuous low doses of nitroglycerin by patch or intravenously produce headache in normal male subjects. MCA velocities were significantly decreased at headache onset and at all levels of headache severity. Changes in MCA velocity persisted beyond the clinical headache. These results suggest a direct MCA vasodilatory effect of nitroglycerin. This method may also be used to evaluate the intracranial hemodynamic effects of other vasoactive drugs, even in clinical settings.

Administration, Cutaneous↗
PubMed1993

Prostaglandin F2 alpha-induced mitogenesis in MC3T3-E1 osteoblasts: role of protein kinase-C-mediated tyrosine phosphorylation.

Prostaglandin F2 alpha (PGF2 alpha) stimulates DNA synthesis in osteoblasts through phospholipase-C-dependent increases in intracellular calcium and protein kinase-C (PKC) activity. We present evidence that stimulation of protein tyrosine phosphorylation by PKC is an additional component of the signaling pathways involved in PGF2 alpha-stimulated DNA synthesis in MC3T3-E1 osteoblast-like cells. Mitogenic doses of PGF2 alpha (42 nM) rapidly induced tyrosine phosphorylation of multiple substrates in these osteoblast-like cells. PGF2 alpha stimulated tyrosine phosphorylation of new proteins with apparent mol wt of 87, 80, 50, 47, 36, and 33 kilodaltons and up-regulated phosphorylation of preexisting tyrosine components with mol wt of 123, 112, 68, and 56 kilodaltons. Stimulation of PKC by 1.6 microM phorbol 12-myristate 13-acetate mimicked the pattern of PGF2 alpha-induced protein tyrosine phosphorylation, whereas PKC-deficient cells (induced by overnight pretreatment with 16 microM phorbol 12-myristate 13-acetate) were refractory to PGF2 alpha-stimulated protein tyrosine phosphorylation and DNA synthesis. The tyrosine kinase inhibitors tyrphostin and genistein blocked PGF2 alpha-stimulated DNA synthesis and protein tyrosine phosphorylation, and the tyrosine phosphatase inhibitor orthovanadate prolonged PGF2 alpha-stimulated tyrosine phosphorylation; these findings are consistent with activation of a putative tyrosine kinase. Calcium/calmodulin antagonists also inhibited PGF2 alpha-stimulated DNA synthesis, but the calcium-signaling pathway played no role in PGF2 alpha-induced tyrosine phosphorylation. Our findings suggest that cross-talk between receptor-mediated activation of PKC and protein tyrosine phosphorylation is an important distal signaling pathway necessary for PGF2 alpha-induced DNA synthesis in osteoblast-like cells.

Animals↗
PubMed1992

PDGF induces tyrosine phosphorylation in osteoblast-like cells: relevance to mitogenesis.

We have studied the association between protein tyrosine phosphorylation and the mitogenic effect induced by platelet-derived growth factor (PDGF) in the osteoblast-like cell line MC3T3-E1. PDGF caused a dose-dependent increase in [3H]thymidine incorporation in MC3T3-E1 cells, reaching a plateau at 10 ng/ml. Vanadate, a potent phosphatase inhibitor, induced a twofold increase in thymidine incorporation. The combination of vanadate and PDGF resulted in a dose-dependent synergistic effect on thymidine incorporation. Genistein, a tyrosine kinase inhibitor, inhibited in a dose-related manner (2-20 microM) the mitogenic effect induced by either PDGF or the combination of vanadate and PDGF. These observations suggest that tyrosine kinases are involved in mediating the mitogenic effect of PDGF in these cells. PDGF treatment of MC3T3-E1 cells and subsequent immunoblotting with antiphosphotyrosine antibodies resulted in a marked phosphorylation of the PDGF receptor. Vanadate had a lesser effect on PDGF receptor phosphorylation, but given together with PDGF it induced a significant increase in the intensity of receptor phosphorylation. Preincubation with genistein abrogated these effects. Taken together, these findings indicate a direct correlation between thymidine incorporation and tyrosine phosphorylation in MC3T3-E1 cells and suggest that tyrosine phosphorylation plays a role in PDGF-induced mitogenic activity in osteoblast-like cells.

Animals↗
PubMed1991

[Platelet hypoactivity in hypocholesterolemia].

A 6-year-old girl with severe malabsorption resulting from pancreatic insufficiency, and with hypocholesterolemia is described. 57% of her plasma cholesterol was found in high density lipoprotein (HDL), 95 mg/dl, while only 25 mg/dl was in the low density lipoprotein (LDL) fraction. Platelet aggregation in platelet-rich plasma, in response to both collagen and ADP, were substantially reduced (by 54 and 33%, respectively) in comparison with normal controls. However, after removal of plasma and washing the isolated platelets, they were not hypoactive. These results suggest that the plasma environment affects platelet activity, and confirms our in vitro results on the enhancing and inhibiting effects of LDL and HDL, respectively, on platelet activity.

Child↗
PubMed1989

Effect of cyclophosphamide and levan treatment on bone marrow and peripheral blood cells in B16-F10 melanoma-bearing mice.

Immunotherapeutic agents have often been found to provoke opposite effects on tumor growth--inhibitory or stimulatory--depending on dose, timing or route of administration. The reason for these opposite effects is not yet known. Levan (polyfructose), an immunomodulatory polysaccharide, has been found to exert opposite effects on the growth of the F10 variant of B16 melanoma. Low doses inhibit and high doses enhance the growth of this tumor. Cyclophosphamide (CY) augments the inhibitory effect of the polysaccharide. In order to elucidate the mechanism of these opposite effects, we tried to determine the changes induced by levan at inhibitory and stimulatory doses, alone or in conjunction with CY, on the lymphatic and hematopoietic systems of B16-F10 melanoma-bearing mice. In a previous study we reported the effect of these treatments on the morphology of spleen and lymph nodes (Leibovici, Kopel, Siegal & Gal-Mor (1986). Int. J. Immunopharmac., 8, 391). In the present study, we examined the effect of the treatments on bone marrow and peripheral blood composition. The growth of the tumor itself, as well as the various treatments, induced very marked changes in both bone marrow and blood. Tumor inoculation produced a sharp leukopenia and anemia followed by a restoration of both white and red blood cells. In the bone marrow, the tumor caused a gradual decrease in lymphocyte number. CY accentuated the severe leukopenia caused by the tumor. Lymphocyte depletion was prolonged, while restoration of granulocytes was achieved by day 7. A similar pattern of changes was observed in the bone marrow. With levan, opposite effects were observed in blood and bone marrow with the two doses in relation to the number of the cells of the lymphoid and myeloid lines: while 0.1 mg (tumor inhibitory) doses caused a more active restoration of lymphocytes as compared to 10 mg (tumor stimulatory) doses, an opposite effect was seen on the myeloid series--the high dose induced a more pronounced granulocytosis than the low dose. In the combined treatment, the low levan dose accelerated lymphocyte restoration in bone marrow compared to CY, while the high dose delayed the recovery of these cells. The results of the present study in conjunction with our previous study may explain the basis of the intriguing tumor inhibitory-stimulatory effects of some immunomodulators. Moderate increases in myeloid cell series appear to favor tumor inhibition and high increases favor tumor stimulation. In addition, the results of this study suggest that a regulatory relation might exist between the proliferation of the lymphoid and myeloid cell series.

Animals↗
PubMed1988

Role of renal prostaglandins in bile-induced diuresis in the dog.

To clarify the possible role of renal prostaglandins (PGs) in the phenomenon of bile-induced diuresis in the dog, we studied the effect of in situ unilateral infusion of bile on kidney function and PGs excretion, before and after PG-synthetase inhibitor administration in anesthetized dogs. The contralateral intact kidney served as control. In the first group of 6 dogs, infusion of bile diluted 1:20 resulted in a significant increase in urinary flow (117%; p less than 0.05), sodium (61%; p less than 0.01), potassium (26%; p less than 0.05), PGE2 (240%; p less than 0.05) and PGF2 alpha (137%; p less than 0.05) excretion rates. Further significant increases in urinary flow, sodium and PGE2 excretion rates were noted with infusion of bile diluted 1:10. All parameters returned to basal levels upon cessation of bile infusion. Significant linear correlation coefficients (p less than 0.005) were found between PGE2 excretion rates and urinary flow (r = 0.72), sodium (r = 0.91) and potassium (r = 0.88) excretion rates. In a second group of 6 dogs, intravenous administration of PG-synthetase inhibitor abolished the increase in renal PGs excretion and the increments in the rates of urinary flow and solute excretion in response to bile infusion. These findings support the notion that the acute diuretic and natriuretic effect of bile, and presumably that of cholemia is mediated, in part, through stimulation of renal PGs synthesis.

Animals↗
PubMed1987

Post-obstructive urinary concentrating defect. A case study in the role of prostaglandins.

A child with post-obstructive urinary concentrating defect was studied for the possible pathophysiological role of prostaglandins and an eventual therapeutic approach. Increased urinary excretion of prostaglandins was corrected by indomethacin, with resultant increased nephrogenous cyclic AMP and partial improvement in the concentrating defect. The addition of a thiazide restored urinary concentration. These results add clinical support to the conception of the important role of prostaglandins in the mechanism of post-obstructive hyposthenuria. This therapeutic regimen is advocated for prolonged post-obstructive concentrating defect.

Child, Preschool↗
PubMed1987

Five-year survey of changing patterns of susceptibility of bacterial uropathogens to trimethoprim-sulfamethoxazole and other antimicrobial agents.

We analyzed the antibiotic susceptibility of 5,348 urinary isolates of Escherichia coli, "Klebsiella aerogenes," and Proteus mirabilis grown in three laboratories from 1980 to 1985. A continuous rise in resistance to trimethoprim-sulfamethoxazole was observed; 63% of the strains from inpatients in 1984 and 51% of those from outpatients in 1985 were resistant to this drug. Isolates from outpatients in 1985 were mostly susceptible to nitrofurantoin (mean susceptibility, 92%) and to oral cephalosporins (mean susceptibility, 84%). As for isolates from inpatients, none of the antimicrobial agents now used was satisfactory for initial chemotherapy, indicating a need for new antibacterial strategies.

Ampicillin↗
PubMed1986

Hypovitaminosis E induced neuropathy in exocrine pancreatic failure.

A 4 year old girl with congenital nerve deafness and pancreatic insufficiency had incapacitating ataxia. Electrophysiological studies of the median nerve and the brain stem evoked response were abnormal. Serum vitamin E concentration was low. After intramuscular injections of vitamin E the ataxia disappeared and electrophysiological variables reverted to normal.

Ataxia↗
PubMed1986

Ultrasonography in the radiologic evaluation of children with urinary tract infection.

A prospective blind study comparing the findings of ultrasonography, intravenous pyelography, and voiding cystourethrography was conducted on 81 patients to examine the place of ultrasonography in the initial radiologic evaluation of children with urinary tract infection. The patients' mean age was 4.8 years; 15 were male. Forty-eight were inpatients (mean age, 3.2 years) and 33 were outpatients (mean age 7.2 years). In 29 patients (35.8%) abnormality of the urinary system was detected by one or more of the three imaging procedures; 21 were inpatients and eight were outpatients. The most frequent finding was vesicoureteral reflux, occurring in 62.1% of the pathologic cases. The findings at ultrasonography correlated well with those of intravenous pyelography in 73 of the 81 studies (90.1%), but they failed to demonstrate double collecting systems and several of the minor changes. However, ultrasonography in combination with cystourethrography identified all patients who had abnormal urinary systems, except for two children with negligible findings. Moreover, ultrasonography and cystourethrography together identified all 11 patients, nine of them inpatients, in whom surgical treatment was indicated. It is concluded that ultrasonography can successfully replace intravenous pyelography as a screening imaging procedure for the urinary system, but because of the superiority of intravenous pyelography in the detection of some types of lesions, intravenous pyelography will be required whenever ultrasonography or cystourethrography results are abnormal.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1986

Oral calcium carbonate as phosphate-binder in infants and children with chronic renal failure.

In view of the known toxicity of aluminum, we studied the effects of CaCO3 as an alternative phosphate binder in 12 chronic renal failure (CRF) children during 152 patient-months. Mean (+/- SD) serum creatinine concentration rose during that period from 3.7 +/- 1.8 to 5.1 +/- 3.0 mg/dl. 8 patients received CaCO3 from the start, and 4 were switched from A1(OH)3 after 2 months of interruption. In addition to CaCO3 (0.1-0.3 mg/kg BW) all patients received NaHCO3, and all but two received 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] or dihydrotachysterol (DHT). Urine and blood variables were checked every 4-6 weeks and medication dosages were adjusted accordingly, aiming to keep serum Ca at 10.4-10.8 mg/dl, serum Pi at 3.5-5.5 mg/dl, and serum HCO-3 above 18 mEq/l. Bone X-rays were obtained every 6-9 months. With treatment, mean serum Ca increased from 8.9 +/- 0.7 to 10.3 +/- 0.4 mg/dl (p less than 0.01), serum Pi decreased from 6.3 +/- 0.9 to 4.2 +/- 0.5 mg/dl (p less than 0.01), and the mean Ca X P product decreased slightly and insignificantly. Mean serum alkaline phosphatase levels decreased significantly from 486 +/- 251 to 168 +/- 28 IU (p less than 0.01). Bone X-rays at the end of the study showed either healing of renal osteodystrophy or its prevention. Only one episode of mild hypercalcemia (serum Ca 11.7 mg/dl) was observed in 1 patient, but his Ca X P product remained low.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Glomerulosa failure in congenital adrenocortical unresponsiveness to ACTH.

We report two children of a family with congenital adrenocortical unresponsiveness to ACTH. Repeated stimulation of the adrenal by Synthetic 1-24 ACTH (Synacthen) failed to increase cortisol secretion, but produced significant rises of serum aldosterone. This was, however, associated with increased plasma renin activity. Only when the renin-angiotensin effect was eliminated, by a converting enzyme blocker, did Synacthen fail to affect serum aldosterone. These data support the view that glucocorticoid deficiency in this disorder results from unresponsiveness to ACTH and that development of the zona glomerulosa and normal aldosterone secretion is achieved by action of the renin-angiotensin system.

Adrenal Cortex↗